Take the Red Pill: The Truth Behind the Biology of Sex

This is the first part of a series about the complex biological realities of sex. Though the posts build on one another, each can be understood alone.

Content note: this post contains images and language that may not be safe for work.

1. Introduction

I first learned about the social construction of sex from a lovely trans woman named Kiki.

She said, “You may have heard before that gender is socially constructed, while sex is biological. But I’m here to tell you that what you’ve heard isn’t true. Sex is socially constructed too. So are you ready for the truth? Are you going to take the red pill or the blue pill?”

Three years later, I was diagnosed by my gynecologist with polycystic ovarian syndrome (PCOS), which means that my body produces hormones intermediate between “typical men” and “typical women.” What I learned from Kiki gave me context in which to understand what this meant about my body and who I am. But it’s still very hard for me to talk about. My hormones affect me in ways that are hard to see, so even most of my lovers don’t know. I can count the number of people in my personal life who know this about me on my two hands.

I picked the red pill. If you read on, you can take the red pill too.

The problem with calling sex “biological” is that biology is complicated. Hardly anything in biology fits into two neat categories like “male” and “female.” To give you an idea of how complicated sexual development really is, let’s go to the very beginning. How do sexual characteristics develop in a human embryo?

2. The Biology

A. Development of the Internal Genitalia

In the sixth week of an embryo’s development, a piece of primordial tissue called the pronephros splits off into a baby kidney and a baby internal reproductive system. This system consists of three parts. There’s the Müllerian ducts, which can develop into fallopian tubes, a uterus, and a vagina. There’s the Wolffian ducts, which can develop into a seminal vesicle, vas deferens, and epididymis. Then there’s the gonads, which can develop into ovaries or testes. At this stage the gonads are called indifferent, which I find kind of hilarious, because I imagine the gonads just chilling inside the embryo going, “Yeah, whatever, I just don’t care about sex differences.”

So what determines what happens to all of these parts? It’s complicated. Very complicated. But I’ll try to cover the highlights.

The embryo doesn’t start to differentiate into male/female traits until 7 weeks in. What determines whether the gonads become testes or ovaries is the presence of a gene called SRY, which is typically found on the Y chromosome (though as with everything in biology, there are exceptions: SRY sometimes wanders off to another chromosome, which means you can have a person with XX chromosomes and testes).

Not everyone has XX or XY chromosomes. Some people have XXY or XYY or XXX or just X. But if the embryo has a Y chromosome, the SRY gene will nudge the indifferent gonads toward becoming testes. This means that even if you have testes, you might not be XY in your chromosomes.

The SRY gene causes some cells in the gonads to begin commitment to sperm development, and to pump out two hormones: the famous testosterone, and the less-known anti-Müllerian hormone, which usually (but not always) causes the Müllerian ducts to break down. (If they don’t break down, the fetus will be born with testes, a uterus, and Fallopian tubes.)

The Wolffian ducts usually develop instead, into the organs that create the non-sperm components of semen and deliver them to the testes. (If they do not develop, this results in an individual with testes who does not ejaculate and is infertile, because the sperm don’t have a nice semen package in which to leave the body.)

In the absence of SRY, some genes on the X chromosome, such as DAX-1 and Wnt-4, kick in. The cells in the gonads commit to egg development. Hormones secreted by the ovaries usually cause the Wolffian ducts to degrade, though sometimes there are remnants. If you have bumps on the sides of your vagina, they may be remnants of the Wolffian ducts you had as an embryo.

The Müllerian ducts usually develop into a uterus, Fallopian tubes, and a vagina, though how much of the vagina comes from the Müllerian ducts is controversial. Don’t you love that there’s a big scientific controversy about vaginas? Scientists aren’t sure whether the entire vagina comes from the Müllerian ducts, or just the upper vagina.

Now, in some cases, the gonads get mixed signals and become intermediate between ovaries and testes, and may be able to produce both eggs and sperm. If that happens, the hormones produced by each part interfere with the other, and the typical result is infertility or only one type of gonad fully functioning. The Wolffian and Müllerian ducts may both develop, one to a side, or just one or the other might develop, or neither.

B. Development of External Genitalia

Meanwhile, on the outside of the embryo, between its tiny growing legs, is a structure that looks like this:

The development of the external genitalia happens later, in weeks 9 through 12 of development. A complex interaction of hormones determines how the external genitalia develop, which means that there are many possible outcomes of genital development. I’ll try to cover as many possibilities as I can. I will refer to the image above as well as the image below, called the Prader scale, which shows some of the different ways the external genitalia can develop.

Picture links to source (warning: describes variation in sex development with pathologizing language.)

Part 1 is the sensitive head of what anatomy textbooks call the “genital tubercle” but I prefer to call the “phalloclitoris,” because as we will see, the penis and the clitoris are so similar that in this story (and maybe in general) it doesn’t really make sense to call them different things. The development of the head of the phalloclitoris is mostly the same in everyone. Testosterone causes it to get larger, but it has just as many nerve endings no matter how big or small it ends up.

Part 2 is a membrane that gives rise to the urethra and the anus in everyone, and to a vagina in some. The first thing that happens to structure 2, in everyone, is that the bottom part pinches off into an anus. What remains is called the urogenital sinus. In some individuals, the story ends there. They have one opening, from which they pee, but also has erotic nerve endings and produces lubricant (though it is often shallower than a vagina; see stage 3 in the Prader scale.) In some individuals, it pinches off into a urethra and a vagina. In the remaining group, it closes up like a zipper into just a urethra. If these individuals have a penis, the urethra usually lengthens up to the tip (but it might not migrate all the way up; see stage 4 in the Prader scale).

Part 3, in everyone, forms the body of the phalloclitoris. Now, here’s where things can get hard to explain, because sex education in this country is woefully inadequate. It is obvious to most everyone what the body of the penis looks like: it’s the shaft, everything that isn’t the head. But not everyone is aware that the clitoris has a body too, not just a head. In most individuals who have a clitoris, only the head is externally visible. But the body of the clitoris is just as long as the body of the penis. It looks like this:

Those four balloon-like things around the vagina are the body of the clitoris. A penis is just like this, just external and sewn up along the bottom edge. Except, of course, not always: some people are born with an external phalloclitoris that opens up along the bottom, like the clitoris in the image above. This all comes from structure 3 in the picture. Structure 3 can also develop labia minora. Anyone who has been sexy-intimate with labia minora, their own or someone else’s, won’t be surprised by this: both the body of the phalloclitoris and the labia minora feel very good when stimulated.

Part 4 can swell into labia majora, or fuse together along the bottom edge into a scrotum. Or something in between can happen: labia majora that form “pouches” like a scrotum, or a scrotum that doesn’t completely seal up along the middle. See the Prader scale image for some of the different ways Part 4 can develop.

That’s it for the external genitalia. The last part of sexual development happens around week 26: the descent of the gonads. You may have heard about the descent of the testes. If a fetus with testes has a scrotum, most of the time, the testes will descend into it before birth. If the fetus has testes but no scrotum, or the signal to descend never reaches the testes, they will remain in the abdomen undescended, possibly for the rest of the person’s life, possibly not. What you may not know is that the ovaries (usually) descend too. When the ovaries descend, they attach to the ends of the Fallopian tubes.

3. The Implications

Those are the biological facts of sexual development. It should be clear to you now that the outcomes of sexual development don’t fall into two obvious categories of male and female. One implication that jumps out at me is that while we don’t know how a sense of gender identity develops in the brain, because there are so many possible outcomes of sexual development in the genitalia, it wouldn’t surprise me at all if we find that there are many possible outcomes of sexual development in the brain. The likelihood of someone growing up to have a penis and a strong sense of female identity is at least as high as someone growing up to have a beard and a vagina, or testes and a uterus.

Another implication is that “biological sex,” in reality, is a spectrum, or maybe even more complicated than a spectrum. However, societies divide this spectrum into socially constructed categories: sexes.

So where do we draw the dividing line? This may seem arbitrary to you, and it absolutely is. Not all societies have divided up this spectrum the same way. For example, in India, some people with genitals in between the typical male and typical female are classified as a third sex, hijra. Where does Western society draw the line? Until the 2000s, the standard was basically this: is the location of the urethra in right place, and the size of the phalloclitoris big enough, that the baby can eventually stand to pee, and be able to insert the phalloclitoris into a vagina?

Even if you are not a regular reader of this blog, the ideology of sex and gender behind this dividing line should be clear. For decades, the medical marker of maleness was a penis that fit the standards of masculinity: standing to pee, and having heterosexual intercourse. These standards had serious consequences. Any baby with a phalloclitoris that didn’t meet medical standards was subjected to unnecessary surgery to reduce the phalloclitoris to an “acceptable” size for a clitoris, raised as female, and kept in the dark for the rest of their life about the genitalia they were born with. These days, the standard used for assigning sex to intersex babies is chromosomal sex. XX, you’re female, XY, you’re male.

But there’s more. While some babies are born with genitalia ambiguous enough for parents and doctors to get into a kerfuffle, there are many intersex conditions that have nothing to do with external genitalia and may go undetected. For example, there are those individuals with XX chromosomes and a wandering SRY gene attached to their genomes somewhere. Those people may manifest, in their gonads, internal genitalia, and external genitalia, as typical males. But until they get karyotyped and have a look at their chromosomes, they may never know they are intersex. There are also conditions that cause male-assigned people to produce high amounts of estrogen and related sex hormones or female-assigned people to produce testosterone and related sex hormones. The effects of these sex hormones are sometimes highly noticeable, but sometimes they are harder to detect.

This means that even if you don’t think you are intersex, you could be. I know because it happened to me.

When I was 18, I was diagnosed with PCOS, polycystic ovarian syndrome. This happens when the ovaries produce unusually high levels of androgens (male sex hormones). PCOS is not classified by the medical community as an intersex condition. However, what the medical community designates as “intersex” or not is motivated by politics, not biological facts. The goal of the way variation in sexual development is defined is to label as few people “intersex” as possible, so they don’t have to live with the “shame” of the diagnosis. The only conditions that are called intersex are ones that can’t be explained away to a child’s parents as a “slight genital abnormality.” Thus, doctors are able to claim that only 1 in 1500 babies is born intersex.

A much more pragmatic definition of intersex, as proposed by Dr. Cary Costello at the University of Wisconsin-Milwaukee, is when a body does not fully differentiate into male or female. By that definition, people with PCOS are intersex, because the condition we were born with makes our androgen levels higher than most women’s and lower than most men’s. Our androgen levels also reduce the levels of female sex hormones in our bodies so that they are intermediate between the typical levels for men and women. Our bodies are not fully hormonally differentiated between male and female. It is thought that up to 5% of female-assigned people may have PCOS. That would mean that at least 1 in 40 people are intersex. The medical community, and society at large, is not ready to accept that figure. If 1 in 40 people don’t fit into our boxes of “biological sex,” then there’s no way to deny that our boxes don’t do a very good job of classifying people. Many people would find that frightening.

I don’t find it frightening. I find it delightful. I am so happy that there is so much sexual diversity in the world, and that biology is too complex and beautiful to jam into two little boxes. When I was diagnosed with PCOS, I wasn’t horrified or scared. I was relieved. Finally, I had an explanation for why my body never followed anything resembling a regular menstrual cycle. I knew why my sex drive would suddenly, drastically change: my hormones were shifting from a female sex hormone-dominated bouquet to a male sex hormone-dominated one, or vice versa.

When I was diagnosed with PCOS, my gynecologist offered me the option of hormone therapy to make my hormonal profile less androgenic and more typically female. Since I was an adult, I could choose whether to take that option or not. I tried it out for a few months, and I hated it. It changed me in a thousand subtle ways that added up to a profound alienation from my own body. I didn’t feel like myself anymore. So I stopped the hormone therapy and went back to my intermediate, intersex state.

Children who are diagnosed with intersex conditions usually don’t get that choice. Their genitals may be operated on, resulting in permanent loss of sexual function. They may be given hormones for years to feminize or masculinize them, causing some of them to go through a partial puberty at age four. The choice of which sex to assign them to, as I explained above, is utterly arbitrary. Many more intersex children end up identifying as transgender than in the general population, knowing that they were born with the very genitalia that they desperately wish hadn’t been taken from them with a surgeon’s knife.

The entry for Androgen Insensitivity Syndrome, an intersex syndrome that results in intermediate genitalia, on Medscape has this to say about how to treat children with this condition: “The ultimate medical goal of treatment is to restore external genitalia as close to a nonambiguous appearance as possible while retaining full sensation, the ability for sexual satisfaction (to include penetrative intercourse), and, ideally, fertility.”

Maybe some people with Androgen Insensitivity Syndrome want to be nonambiguous. Maybe they want to have penetrative intercourse. But when they’re babies, you can’t possibly know. I remember how miserable I was on the hormone therapy that made me “typically female.” I can’t imagine what it would have been like if I’d been forced to be on them all my life. No one should ever have to go through that. Nonconsensual, unnecessary surgery is morally wrong, and I extend my deepest sympathies to all intersex people who have been violated that way.

You hear all kinds of stories about “biological sex.” At the Olympics, they determine the sex of athletes by measuring their testosterone, because supposedly testosterone is what gives male athletes an advantage over female athletes. You also see scientific studies about how testosterone makes men more aggressive than women, more sexual, better-adapted to be hunters back when they were cavemen. If these stories are true, then I have the advantages of a male athlete. I am aggressive, sexual. I am a caveman hunter. If the way men and women behave is an inevitable consequence of biology, then where do I, and other intersex people, fit in?

We don’t. Because the stories aren’t about us. They aren’t about biology, which is messy and complicated. They’re fables. They’re folk tales we tell each other so we’ll keep believing in the great patriarchal fantasy that there are two sexes that are completely different from each other, and that one is better than the other. Because biology.

Well, I’m a person too. So are other intersex people. So are non-intersex people who don’t fit into the patriarchal narrative of how we’re supposed to live. And this is our story.

Out of curiosity, whats your day job, that you enjoy slinging non-normative gene and embryology goodness about? Or more of a longstanding interest? This piece could do (is doing) a lot of good as a way to approach sex.

” I would like to preface this comment by saying that I’m not an expert on the topic or even on human biology, while the author mentions that she is in a STEM field; however, my mom just finished out 40 years as a NP in OB/GYN and a large portion of her focus over the last decade has been working with women with PCOS.

The author is right that the medical community expects that there is a much larger percentage of female-identified people who have the syndrome than has been identified. However, I don’t think that necessarily follows to the conclusion that the medical community is scared of labeling people as intersex, mainly because excess androgen activity is not actually a requirement for an individual to be diagnosed as having PCOS. Currently a PCOS diagnosis is based on having two of three symptoms: irregular or no periods, excess androgen activity, and/or polycystic ovaries. It is possible to be diagnosed with PCOS and not have androgen over-expression; it is also possible to have PCOS and not have polycystic ovaries. There is a movement to redefine the syndrome as all three symptoms rather than just two, which would obviously narrow the population who would be defined as having PCOS. Additionally, many individuals with PCOS do not know that they have it and most will go undiagnosed unless they suffer from another symptom (excess body hair, extremely irregular periods, hypofertility).

Furthermore, I strongly object to the assertion that by Dr. Costello’s definition, “people with PCOS are intersex, because the condition we were born with makes our androgen levels higher than most women’s and lower than most men’s.” The author makes no scientific argument to support the idea that PCOS (which is a syndrome describing a constellation of symptoms, not a single identified condition) is inherent at birth. For me, this raises the question of whether or not the author believes that people with PCOS change sex at puberty, since most sex hormone production clicks on at that stage, and the majority of people have already identified as one sex or another (whether by reasonable standards or otherwise) by that age.

The author is intersex because she identifies as such. I am glad that she feels her identity so strongly and that her diagnosis helped her come to this identity. I am hurt by her following assertions that all people with PCOS have this same identity because I have PCOS and I do not share it.”

I expected to get a comment like this, because I’m well aware of the disagreements surrounding the definition of PCOS and I didn’t have room to address them in the post. My gynecologist who diagnosed me defined PCOS by the stricter definition you gave, and called the less strict definitions just “PCO”, polycystic ovaries. I’m not a doctor, but it may be relevant to differentiate the diagnoses, as people with more androgenic hormones face some unique issues – the same issues that most intersex people have in common.

The case of PCOS is not the only one supporting the idea that doctors try to avoid classifying conditions as intersex. I refer to the posts on Dr. Costello’s blog about how hypospadias (conditions wherein people are born with testes, a urogenital sinus somewhere between the perineum and penile shaft, and an intermediate labioscrotum) are not defined as intersex, even though they have intermediate genitalia. I can only conclude that this is because people with hypospadias are surgically assigned as male and doctors want to spare them the “shame” of an intersex diagnosis, as I posited in the post.

There is in fact a lot of evidence that PCOS is genetic (Strauss 2003, Annals of the New York Academy of Science). My current gynecologist has been in the business for decades and has observed that it runs in families; many other gynecologists have observed the same.

Polycystic ovarian syndrome is a genetic condition that becomes manifest at puberty, often results in intermediate secondary sex characteristics, represents an intermediate hormonal phenotype, and affects the size of the gonads.

Congenital adrenal hyperplasia is a genetic condition that often becomes manifest at puberty, results in intermediate secondary sex characteristics, and represents an intermediate hormonal phenotype.

Klinefelter syndrome (XXY chromosomes) is a genetic condition that usually becomes manifest at puberty, often results in intermediate secondary sex characteristics, represents an intermediate hormonal phenotype, and affects the size of the gonads.

The latter two conditions are considered intersex, while the first is not. Why? The distinction seems completely arbitrary to me. I am definitely not in the business of telling other people how to identify, but I think it would be beneficial for people with PCOS and the intersex community at large if PCOS were identified as intersex, because we have many concerns in common. People with PCOS often present with masculine secondary sex characteristics and face discrimination along with other intersex people for presenting as physically somewhere between male and female. We are also faced with the choice (or, sadly, lack of choice) about whether to take hormone therapy to make us conform with our “biological sex”, as other intersex people are. Thus we can unite to fight for our rights that have been stolen from us by a society that requires the myth of two inviolable sexes for the substantiation of patriarchy.

But again, it is your choice. There are also many people diagnosed with Klinefelter syndrome or something else considered intersex by doctors who do not identify as such, and I support everyone’s right to define their own bodies.

PCOS, in many people, does change the assigned female at birth (afab) body to a more masculine one. The testosterone increase (if present- as it is in my condition) changes the way your body handles fat storage. On typical female bodies, fat is mostly stored in the hips and thighs and buttocks, generally considered a good thing as its useful during pregnancy for some reason (you’ll have to google that for more information). In high testosterone female bodies, fat is concentrated around the stomach- have you ever seen a larger man with a “beer belly?” That’s what happens in overweight PCOS high testosterone female bodies. For me, this is incredibly upsetting, I’d give anything to have a more feminine fat distribution. I look at pictures of plus sized models in clothes that will never fit me because the shape of my body is male.

Also, and this was already noted, the excess hair is noticeable. If I didn’t control it, I’d have a beard, something I don’t want. I’m currently on hormone treatment because my body refuses or cannot give me hormones to make me look like the social idea of a woman. The hormones I take serve two purposes, one is to control the menstrual cycle, and one is to control the hair growth. The fact that this is necessary is evidence of a difference of secondary sex characteristic

Yes, no one PCOS case is the same, but the hair and fat distribution is common, as well as male pattern baldness, which is something I don’t have (which to me is a blessing I don’t have that gene).

So no, I don’t have statistics for you, in the research I’ve done on the issue I’ve never found stats other than 1 in 20 women (and that number is debated) are thought to have PCOS. To be honest, I find it insulting and insensitive that you need to ask for proof (particularly that you asked for photos) to confirm that PCOS bodies look different than typical afab bodies, and I really think you should consider what you’re asking for when you ask real people to prove their bodies are the way they are.

I never once said that these PCOS women don’t exist, I was just questioning why we should jump to calling ourselves intersex because of 1. characteristics we may or may not have and two characteristics that are easily shared in other women who do not have PCOS. Is every woman who is more of an apple shape, or women who grow body hair in other places outside of the typical grouped in too? Are PCOS women who have socially acceptable feminine bodies or less hair growth grouped in also? How do we characterize those who’s PCOS manifested later in life? If diet and lifestyle changes are able to lessen your PCOS symptoms and balance your hormones are you still intersex or does it change again?

I asked for proof to understand why a syndrome that is notorious for having so many different manifestations within us is being use to determine what sex you may be based on things that may or may not exist within them and exist outside of the pcos community. That’s it. It didn’t make sense to me, and since the burden of proof isn’t on me…

If that makes you feel bad, I apologize. But you can’t make blanket assertions based on a multi-faceted, and oddly manifesting syndrome about the sex of people you don’t even know based on your personal experiences and observations without someone looking for more backup than “Well these are the ‘typical symptoms'”

Regardless I am done here. I got my answer of “what I was saying was kind of out of my ass” from the author so there is no reason for me to even continue knowing the place from with the assertions came.

characteristics we may or may not have and two characteristics that are easily shared in other women who do not have PCOS.

Actually this is true of many intersex conditions. As stated above, congenital adrenal hyperplasia can result in hirsutism, an enlarged clitoris, and male-pattern muscle growth, and it is considered an intersex condition. But there are dyadic typical women who are hairy, have a large clitoris, and male-pattern muscle growth. Just because the same characteristics can appear elsewhere in the population doesn’t mean it’s not intersex.

I’m not telling you to self-identify as intersex. As I said, defining your own body is important. I’m just saying that it could be very helpful and useful for there to be allyship and cross-identification between the PCOS and intersex communities – for some people, including some other commenters on this post.

Overall I found the article to be quite accurate and well done. Brovo!

I should point out a tiny error that tends to be a common misconception. I noticed it in the statement reading “…non-sperm components of semen and deliver them to the testes.” That would involve a backwards flow of semen fluid in the vessels. The fluid is secreted along the path the sperm flows during the process of ejaculation.

It’s about a series of experiments in which ewes were prenatally exposed to testosterone, and ended up with something very similar to PCOS.

From the Discussion near the end of the paper:
“Evidence from prepubertal androgenized lambs suggests that folliculogenesis is abnormal in these lambs, and this is manifest as enlarged, multifollicular ovaries … Of interest is the observation that the compromised feedback and multifollicular morphology of ovaries from T60 ewes are remarkably similar to those found in women with disorders of androgen excess, such as polycystic ovary syndrome and congenital adrenal hyperplasia (36, 37, 38). Polycystic ovary syndrome is a disorder associated with abnormal follicle development, hyperandrogenization, and hypersecretion of LH and is probably the most common cause of anovulation in women of reproductive age (36). Many of these characteristics are also displayed by female sheep androgenized in utero (10, 32, 33, 34, 35, 39), raising the possibility that prenatal androgen exposure could be a developmental factor implicated in the etiology of this common disorder.”

I suffer from secondary hypogonadism, which is the male equivalent of PCOS – my brain is regulating my testosterone production to too low a level, with the result that I’ve developed a body that looks a bit like a cross between a man’s and a woman’s, and more recently, have become quite sick due to my testosterone falling to such a low level. I think all this happened as a result of being prenatally exposed to synthetic female hormones. I’ve discovered that there are loads of nominally male people about who were exposed to a synthetic estrogen called DES, and have similar symptoms to myself. My theory is that artificial estrogens (such as DES) can cross the placenta and block testosterone production in a developing male fetus, with the result that you get intersexed or completely female development taking place during the time it’s being administered. Because most exposure to medical hormones takes place after the end of the first trimester (by which time genital development and development of the reproductive organs has already finished), you end up with a person whose physical appearance is male, but whose brain has undergone varying degrees of female development. Most of the DES “sons” I’ve had contact with have had so much of their brain development go down the female pathway that they’ve ended up trans. Now I know what it is, I can tell that part of my brain development has occurred as female too, although in my case a fair bit is male as well, so I don’t identify as a woman.

While I was finding out about DES and estrogens, I discovered that there’s a second class of hormones called progestins, that have also seen a lot of use during pregnancy. Although they’re supposed to be mimicking a female hormone, the early progestins were all derived from the testosterone molecule, and turned out to have quite strong androgenic effects on female fetuses (see the wikipedia article on Progestin-Induced Virilization). Maybe your mother was given one of these hormone treatments while she was pregnant with you? Millions of people were prenatally exposed to DES. I haven’t been able to find any stats on progestin use, but looking at the medical literature, they seem to have commonly been co-prescribed with DES from about 1950 onwards. DES had largely been withdrawn from use by about 1980, but some progestins are still used in pregnancies where the mother has symptoms of threatened abortion or a history of premature birth.

I think the pharma industry have, for several decades, been quietly sitting on a colossal intersex disaster caused by these drugs, but I guess the numbers exposed and the potential liability are so large, that everyone involved is trying to keep the whole thing a secret. I’ve been trying to get the story into the news, so far without success unfortunately.

I think the problematic language is this: “By that definition, people with PCOS are intersex” — it actually kinda does seem like you’re telling people how they should ID.

Many people with PCOS may ID as intersex, and I like the idea of opening the definition up a bit, but I (as someone with hormone-level-diagnosed PCOS) do not feel comfortable doing so, because as long as I pluck my beard I so easily pass as cisfemale.

Thank you for this article. I have PCOS and found your insights to be very helpful in understanding my own identity dilemmas. I have been on high dose estrogen birth control for about a decade now, and it works well for me, but this sheds light on the way my identity seemed to change frequently, especially during puberty.
A major reason I started the birth control was due to my doctors saying I’d have an increased risk of developing heart disease and diabetes if I did not treat the condition by balancing out my hormones. Is this something to consider for people who do not wish to take hormones, or do these assertions require more research?

Your doctors are correct. Heart health and diabetes are tied to the balance of sex hormones in people with PCOS. When I gave up the hormone therapy (I don’t think of it as birth control because I wasn’t using it to control fertility) I started paying a lot more attention to my diet and exercise. My doctors agreed that as long as I kept up my stringently good habits, I would be fine without the hormone therapy. That’s not to say that what I did is the right decision for everyone with PCOS, but it was right for me.

your mention of hijra here is a little misleading imo. it can be used to refer to intersex people but it’s more inclusive than that, it can also be used to refer to some of what english-speaking countries would call transgender people, or people who adopt a specific cultural gender identity

I like those graphics a lot. They do a good job of explaining congenital adrenal hyperplasia. I don’t think they’d’ve worked for the article, though, because they assume that the baby has a uterus. The scale can also apply to intersex babies who don’t have a uterus.

A very well-written and thought-provoking piece! As a geneticist I really enjoyed reading through it and learning more about the developmental side!

I’d just like to raise the point though that from a purely scientific view, sex (as opposed to gender) never has been labeled as a binary system. In the strictest definition, sexual males are those who produce small mobile gametes and sexual females are those that produce large, mostly stationary gametes.

However, nowhere is it written that individuals (whether they be humans, other animals or even plants) have to be just one category or another. Indeed pretty much all flowering plants produce both pollen from stamen and ovules in the ovary. The commonly-used model organism C.elegans (nematode worm) also exists almost entirely in hermaphroditic form producing both forms of gamete whilst there are species of fish, for instance, that change sex from female to male (stop laying eggs and start making sperm) during their lifespan based on the sexual diversity of their population.

Hence whilst I fully agree with you that there is no such thing as two boxes that everyone should be expected to fall into, I think it’s tricky to argue that there is a full spectrum of sex, as the issues you raise with regard to translocations and other genetic complications may well affect genital development but don’t necessarily alter the gametic definition of sex.

I’d love to get your insight on this, huge congrats for a quality article!

I don’t find this concept scary at all. It delights me. And what a surprise – messy, evolved, random and *wet* biology turns out to be totally non binary. Everything is on a spectrum – or a hugely complex multi dimensional cube of possible categories. Or, perhaps, and this could be utopia: no categories at all.

The sooner we, as a society, learn this, and embed it in our consciousness and ways of thinking, the sooner we can fully accept and embrace everyone, regardless of how or what they are.